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Antibiotics for OCD

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My Google alerts brought me this story. I'd heard about the use of d-cycloserine for pediatric OCD more than a year ago when Dr. Storch mentioned it at the IOCDF conference, but I'm glad to see the information hit a broader media.

 

Antibiotic for Pediatric OCD

 

But what really struck me about this story was the description of the boy in the story, Ben: "Making matters even worse for Ben is he has attention-deficit hyperactivity disorder (ADHD) and Tourette’s syndrome. Tourette’s can happen at times in children with OCD."

 

OCD, TS and ADHD? Does Ben's mom know about PANDAS? And being in a study at USF, wouldn't bells go off for Storch and his team, given the comorbidity symptoms? Oh, and Ben is responding to antibiotics?!?! Is anyone here surprised by THAT?

 

Some of you know the folks at USF far better than I do. How would a child like this go through the system/program and not be identified or at least tested for PANDAS? Okay . . . maybe I'm jumping the gun. Maybe he was, and there's no clinical evidence of strep, lyme, myco p, etc.

 

Still can't help wondering, though . . . . . . :blink:

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This explains why that antibiotic was chosen

 

http://clinicaltrials.gov/ct2/show/NCT01411774

 

Detailed Description:

 

Obsessive-compulsive disorder (OCD) affects 1-2% of children, runs a chronic course without treatment, and is associated with considerable functional impairment and poor quality of life. Although most patients with OCD respond to cognitive-behavioral therapy (CBT) or pharmacotherapy with a serotonin reuptake inhibitor (SRI), a substantial number of youth remain symptomatic after receiving these therapies. Pharmacological interventions with SRIs are only moderately efficacious, rarely produce remission, may be accompanied by side effects, and may not be an acceptable intervention to some parents. Medication augmentation strategies such as atypical antipsychotics are often used in children with partial response but have concerning metabolic effects and no systematic supporting efficacy or safety data. Although CBT is the gold standard treatment for pediatric OCD, not all patients benefit and the availability of skilled therapists is quite limited. Thus, there is a critical need for interventions to optimize treatment outcome in pediatric OCD. The primary mechanism in CBT is repeated and prolonged exposure to feared situations while abstaining from OCD rituals. This treatment is based on animal models of extinction of conditioned fears. Basic research on the neural circuitry underlying fear extinction led to the examination of d-cycloserine (DCS), a partial agonist at the NMDA receptor in the amygdala, as an agent capable of enhancing extinction learning. Following successful validation of this strategy in animals, six trials in adult humans - and one study in youth with OCD - provide support for DCS dosing as facilitating extinction learning that occurs during exposure-based psychotherapy. However, experts and agencies responsible for regulating drug indications in the US, including the FDA, recognize that safety and efficacy findings in adults should not be routinely extrapolated to children. The present study furthers pilot work on DCS to augment the effects of CBT in children with OCD. The investigators are conducting a double-blind randomized controlled trial, conducted at two sites, to examine the relative benefit of 10 psychotherapy sessions of which sessions 4-10 will be augmented with weight-adjusted doses of DCS (25/50mg) compared to CBT augmented with placebo. 150 youth (ages 7-17) with OCD will be randomly and evenly assigned to one of the two treatment conditions. The primary outcome will be change in OCD symptom severity assessed by independent evaluators. The study recruitment sites are the University of South Florida (USF) and Massachusetts General Hospital/Harvard Medical School (MGH). This study extends the first report of DCS augmentation in youth with anxiety disorder/OCD by conclusively investigating an innovative research approach that manipulates glutamatergic pathways to mediate improved outcomes of exposure-based psychotherapy based upon a translational model of the neurobiology of OCD.

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This explains why that antibiotic was chosen

 

Basic research on the neural circuitry underlying fear extinction led to the examination of d-cycloserine (DCS), a partial agonist at the NMDA receptor in the amygdala, as an agent capable of enhancing extinction learning.

 

The study recruitment sites are the University of South Florida (USF) and Massachusetts General Hospital/Harvard Medical School (MGH). This study extends the first report of DCS augmentation in youth with anxiety disorder/OCD by conclusively investigating an innovative research approach that manipulates glutamatergic pathways to mediate improved outcomes of exposure-based psychotherapy based upon a translational model of the neurobiology of OCD.

 

Thanks for the detail, Vickie. Yes, I know why that specific abx was chosen; in fact, it was actually used many years ago on adult OCD patients and the positive results were documented, but when they couldn't be replicated, the study was somewhat discredited (sound at all familiar?).

 

I added some bolding here pertaining to the "glutamatergic pathways" piece of the puzzle. D-cycloserine isn't the only antibiotic known to have impact on the glutamatergic pathways; beta-lactam abx are also being studied for that activity, and that class includes penicillin, amoxicillin and Augmentin, three of the abx frequently used to treat PANDAS.

 

I'm tempted to drag my soapbox out again, sorry. :P But these frequent and fairly consistent "overlaps" of the "OCD World" and the "PANDAS World" needle at me. Maybe these two conditions are not as far apart as was once believed?

 

And I'm still curious about the very PANDAS/PITANDS-like symptom set of the boy in the story. :huh:

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This explains why that antibiotic was chosen

 

Basic research on the neural circuitry underlying fear extinction led to the examination of d-cycloserine (DCS), a partial agonist at the NMDA receptor in the amygdala, as an agent capable of enhancing extinction learning.

 

The study recruitment sites are the University of South Florida (USF) and Massachusetts General Hospital/Harvard Medical School (MGH). This study extends the first report of DCS augmentation in youth with anxiety disorder/OCD by conclusively investigating an innovative research approach that manipulates glutamatergic pathways to mediate improved outcomes of exposure-based psychotherapy based upon a translational model of the neurobiology of OCD.

 

Thanks for the detail, Vickie. Yes, I know why that specific abx was chosen; in fact, it was actually used many years ago on adult OCD patients and the positive results were documented, but when they couldn't be replicated, the study was somewhat discredited (sound at all familiar?).

 

I added some bolding here pertaining to the "glutamatergic pathways" piece of the puzzle. D-cycloserine isn't the only antibiotic known to have impact on the glutamatergic pathways; beta-lactam abx are also being studied for that activity, and that class includes penicillin, amoxicillin and Augmentin, three of the abx frequently used to treat PANDAS.

 

 

Can you explain this in simpler terms? Is this why my son's OCD gets worse when he goes off of antibiotics? What is the augmentin xr doing?

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Can you explain this in simpler terms? Is this why my son's OCD gets worse when he goes off of antibiotics? What is the augmentin xr doing?

 

Honestly, I'm not sure what the Augmentin XR is doing in totality, but my DS, like yours, has an increase in his OCD behaviors and overall anxiety without it. And Sammy Maloney experienced the same phenomenon, according to his mom, Beth.

 

I don't know definitively that it has anything to do with the glutamate modulating properties of the Augmentin, but I do know that it is a possibility. There are studies currently underway at Johns Hopkins pertaining to the glutamate modulating properties of the beta-lactam class of antibiotics. Dr. Rothstein at Johns Hopkins has studied and written on it extensively.

 

Basically, increasingly, researchers and scientists think that a key component of some "mental illness" and mental conditions, is an imbalance of the neurotransmitter glutamate in certain parts of the brain. Improper glutamate modulation is now being associated with everything from OCD to ALS to autism to schizophrenia and bipolar disorder. A scientist in Detroit (Dr. Rosenberg at Wayne State) found through brain imaging that kids with OCD tend to have excessive levels of glutamate in the caudate nucleus of their brains, which is one of the sections of the basal ganglia that Drs. Swedo and Cunningham have noted as being enlarged in PANDAS kids. There's currently an ongoing trial via the NIMH now for riluzole, a glutamate modulating drug currently FDA approved for the treatment of ALS, for combatting OCD; they're finding some good results, according to Dr. Grant, who's in charge of the trial. Meanwhile, many of the families here on the forum have found some success with glutamate-modulating supplements for our kids' OCD behaviors: NAC, B12, Namenda, Lamictal, even Delsym cough suppresant.

 

So, is the Augmentin contributing to this process? I've corresponded with Dr. Rosenberg at Wayne State and Dr. Grant at NIMH, hoping one or both of them would take interest in the topic of abx's glutamate-modulating properties, but they're both committed to other areas of the glutamate research now: Rosenberg with genetic predisposition toward glutamate levels, and Grant with the riluzole answer. But Dr. Grant said that he found the possible intersection of abx treatment for PANDAS and glutamate modulation via b-lactam abx "intriguing." My next stop is Rothstein at Johns Hopkins, but I haven't found a "way in" there as of yet. ;)

Edited by MomWithOCDSon

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Thanks Nancy!

 

In our case, NAC and B12 cause bad reactions while Augmentin is a miracle drug. Is it a glutamate issue in our case or not???? Wish I knew the answers. :(

 

Well, I just today was given some new research information regarding NAC that might go some way toward explaining "bad reactions" to it; I have to credit LLM for stepping in and giving me some info. Apparently, NAC has been found to be a "biofilm buster," so possibly, if a kid has a bad reaction to NAC, it could be about a "herx" reaction from the biofilms that harbor bacteria being disabled, and then that microbial trigger being released. Here're a couple of links on the topic:

 

NAC Busts Biofilms on Surfaces

 

NAC and Biofilms

 

I guess, as with any herx reaction, then, someone might get worse before they get better while taking NAC.

 

As for B12, we have to be careful with its dosing also, but on our end it seems to be because my DS is already high in histamine, and B12 further increases histamine. And if you Google "histamine" and "brain function," you'll get a lot of hits about how histamine . . . and too much of it and/or too little of it . . . can impact the CNS. So, in that case, it may be about finding the right balance. From the anecdotal evidence, it would appear that decreasing glutamate at the expense of increasing histamine, at least for people with adequate or excess histamine to begin with, isn't necessarily a good trade-off. <_<

 

Again, thanks LLM for the new research info! You must've been psychic and could see these discussions coming down the pipe! :P

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Nancy--You are amazing--

Thank you for pulling these threads together re: possible reasons that antibiotics are affecting the OCD issues. Let's hope that there is (someday) a large scale study to prove the point that antibiotics may have a positive effect on OCD.

 

So then, along that same line, does anyone know: if a child has "Pitand" issues, no strep, but OCD/perseverations that appear when they are exposed to illness (even illness in others, especially strep!)...then would or why might IVIG or pex work???

 

Would immunomodulating treatments (IVIG or PEX) still hold "promise" of resetting the system (so to speak) if the root cause is glutamate issues???

 

Help!

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So then, along that same line, does anyone know: if a child has "Pitand" issues, no strep, but OCD/perseverations that appear when they are exposed to illness (even illness in others, especially strep!)...then would or why might IVIG or pex work???

 

Would immunomodulating treatments (IVIG or PEX) still hold "promise" of resetting the system (so to speak) if the root cause is glutamate issues???

 

Help!

 

Key questions! If only we had our own personal research staff that we could feed all these "What if's" to, and they would take them and run! :P

 

Again, synchronicity is in abundance today, for some reason (I should check my horoscope :lol: )! I got another Google alert tonight regarding "glutamate," only this story seems to have some response to your ponderings, TMom, in terms of the interplay (if any) between glutamate, auto-immunity (in this instance, as in Chron's disease) and even another "culprit" in our PANDAS/PITANDS realm, inflammation. See what you think about this story:

 

Anti-inflammatory Against Glutamate

 

So maybe there are relationships that are only beginning to surface? In which case, I guess what needs to be determined is, once again, the root cause. I had asked both Rothberg and Grant about the whole enlarged caudate (PANDAS)/glutamate-filled caudate (OCD) thing: did the caudate fill with glutamate as found by Rothberg because it was inflamed and provided room for the glutamate to collect, or did the glutamate collection in the caudate itself cause the inflammation found by Swedo? Chicken or egg? Unfortunately, neither would opine on it, saying they're not sufficiently familiar with the other's research on the topic.

 

I wish I weren't so long in the tooth, or I wish I'd known when I was 20 what I know now (or rather, what I DON'T know)! I'd go back to school to try and get some sort of handle on all this and then roll up my sleeves in a lab somewhere myself! :P

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Honestly, I'm not sure what the Augmentin XR is doing in totality, but my DS, like yours, has an increase in his OCD behaviors and overall anxiety without it. And Sammy Maloney experienced the same phenomenon, according to his mom, Beth.

 

I don't know definitively that it has anything to do with the glutamate modulating properties of the Augmentin, but I do know that it is a possibility. There are studies currently underway at Johns Hopkins pertaining to the glutamate modulating properties of the beta-lactam class of antibiotics. Dr. Rothstein at Johns Hopkins has studied and written on it extensively.

 

I understand (sort of) the glutamate-modulating affect, but why was Sammy able to eventually go off the Augmentin XR?

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We have just started my daughter back in a local CBT program after doing Dr. Storch's 3 week program in July. I am going to talk with my local doctor about trying this to see what kind of results we get.

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We have just started my daughter back in a local CBT program after doing Dr. Storch's 3 week program in July. I am going to talk with my local doctor about trying this to see what kind of results we get.

 

Your trick there will probably be dosing. I don't have it in front of me, but I know that the commonly packaged dosage level of d-cycloserine (used for TB) is MUCH higher than the dose Storch et. al. are using with the kids in their research group. So, you would have to get it from a compounding pharmacy or maybe a hospital pharmacy. Perhaps USF can help you with a resource.

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I understand (sort of) the glutamate-modulating affect, but why was Sammy able to eventually go off the Augmentin XR?

 

Like all the other questions, I don't know that anyone really knows. Beth did make a comment in her book about how, at the last attempt at reducing the abx before he was taken off entirely, Sammy was "determined to make it work this time" after a couple of failed attempts at taking him off or reducing it. I asked her what she meant by that, and she admitted that it took some CBT/ERP work on Sammy's part to maintain some of the more stubborn OCD/anxiety behaviors as they reduced the medication.

 

So, in my mind, I'm thinking that it's a possibility that, as they pulled back on whatever support the XR was lending him, since he was overall healthier and better able to make use of the therapy skills he'd been given, he worked hard at staying level, under control, and his body/brain began to regain it's own "natural balance" in terms of the glutamate modulation, as well as other brain chemicals and responses. We've talked on this forum before about how stress/anxiety alone might contribute to the blood brain barrier remaining open when it shouldn't be, allowing stuff to get into the basal ganglia that shouldn't be there. Since excess glutamate is considered an excitotoxin, perhaps it's the case that the brain releases/makes more of that when under stress, as well; many neurons are firing indiscriminately when one is anxious and "ramped up." So it could be sort of a matter of "getting off the merry-go-round" and remaining sufficiently "non-anxious" long enough for existing excess glutamate to be taken up or reduced, and then it becomes possible to reduce external supports.

 

I know we experienced the same "Sammy pheonomenon" the couple of times we tried reducing my son's XR over the last couple of years. More recently, though, after nearly 2 years of solid XR, we decided it was time to try again. He's been in a "good place" for an extended period, so DH and I thought maybe he'd finally gotten off the Anxiety Merry-Go-Round and it was worth another shot. This time we started very slow, though, switching out only his night-time XR dose every OTHER day for a 500 mg. regular Augmentin for about 1 month; 3 weeks ago, now, we shifted down again to giving him that 500 mg. dose EVERY night. He's had a couple of atypically anxious moments in the last couple of weeks, but he's recovered reasonably quickly, and we haven't seen the spiraling down into the abyss sort of trend that we'd seen in previous reduction attempts (knock on wood). So, this time, we're sticking with it. Once he seems entirely level at this dosage, I'm hoping we can reduce again, swapping out a morning dosage of XR for a 500 mg. regular augmentin, first every other day, and then hopefully every day, until we take him off altogether.

 

I don't know what the answer is; I'm just trying to put together the experiences others have shared, the current research available that's at all understandable to a non-science person like me, and our own experiences.

 

Anybody else have thoughts on this topic?

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Like all the other questions, I don't know that anyone really knows. Beth did make a comment in her book about how, at the last attempt at reducing the abx before he was taken off entirely, Sammy was "determined to make it work this time" after a couple of failed attempts at taking him off or reducing it. I asked her what she meant by that, and she admitted that it took some CBT/ERP work on Sammy's part to maintain some of the more stubborn OCD/anxiety behaviors as they reduced the medication.

 

So, in my mind, I'm thinking that it's a possibility that, as they pulled back on whatever support the XR was lending him, since he was overall healthier and better able to make use of the therapy skills he'd been given, he worked hard at staying level, under control, and his body/brain began to regain it's own "natural balance" in terms of the glutamate modulation, as well as other brain chemicals and responses. We've talked on this forum before about how stress/anxiety alone might contribute to the blood brain barrier remaining open when it shouldn't be, allowing stuff to get into the basal ganglia that shouldn't be there. Since excess glutamate is considered an excitotoxin, perhaps it's the case that the brain releases/makes more of that when under stress, as well; many neurons are firing indiscriminately when one is anxious and "ramped up." So it could be sort of a matter of "getting off the merry-go-round" and remaining sufficiently "non-anxious" long enough for existing excess glutamate to be taken up or reduced, and then it becomes possible to reduce external supports.

 

I know we experienced the same "Sammy pheonomenon" the couple of times we tried reducing my son's XR over the last couple of years. More recently, though, after nearly 2 years of solid XR, we decided it was time to try again. He's been in a "good place" for an extended period, so DH and I thought maybe he'd finally gotten off the Anxiety Merry-Go-Round and it was worth another shot. This time we started very slow, though, switching out only his night-time XR dose every OTHER day for a 500 mg. regular Augmentin for about 1 month; 3 weeks ago, now, we shifted down again to giving him that 500 mg. dose EVERY night. He's had a couple of atypically anxious moments in the last couple of weeks, but he's recovered reasonably quickly, and we haven't seen the spiraling down into the abyss sort of trend that we'd seen in previous reduction attempts (knock on wood). So, this time, we're sticking with it. Once he seems entirely level at this dosage, I'm hoping we can reduce again, swapping out a morning dosage of XR for a 500 mg. regular augmentin, first every other day, and then hopefully every day, until we take him off altogether.

 

I don't know what the answer is; I'm just trying to put together the experiences others have shared, the current research available that's at all understandable to a non-science person like me, and our own experiences.

 

Anybody else have thoughts on this topic?

 

Nancy, awesome to hear that the dose reduction is working better this time. We're trying something similar, but too soon to tell. Please keep us posted!

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